One mechanism by which activated RTKs might cooperatively contribute to tumor cell survival is by engaging overlapping downstream effectors. If this were true, then the inhibition of any one RTK pathway would be insufficient to negate the effector due to inputs from the remaining activated RTKs. Because our data show that the spectrum of co-activated RTKs in tumors varies considerably from patient-to-patient, targeting these node effectors might be a more tenable therapeutic alternative to inhibiting RTKs. Moreover, the identification of these downstream effectors should reveal important novel mechanisms whereby RTKs confer their downstream effects. Our lab is identifying these convergent effectors and characterizing their modes of action through phospho-proteomic profiling, genetic and pharmacogenetic screens, in silico network analyses, and in vivo intracranial tumor generation.